A renal transplant recipient presents 20 months post-transplant with slowly rising serum creatinine over several weeks, now 210 micromol/L. Biopsy shows marked thickening of the arterial intima by proliferating smooth muscle cells and connective tissue, causing luminal narrowing, with interstitial fibrosis and tubular atrophy. There is no dense interstitial inflammatory infiltrate. What is the underlying process?
- A Chronic rejection with transplant vasculopathy ✓
- B Acute cellular rejection, Banff grade IIA
- C Calcineurin inhibitor toxicity with nodular arteriolar hyalinosis
- D Recurrent IgA nephropathy
Correct answer: A. Chronic rejection with transplant vasculopathy
Explanation
The hallmark lesion of chronic rejection is transplant arteriopathy: concentric intimal proliferation of smooth muscle and matrix in arteries, producing ischemic glomerulosclerosis, interstitial fibrosis and tubular atrophy. Acute cellular rejection shows interstitial lymphocytic infiltrates and tubulitis. Calcineurin inhibitor toxicity produces striped fibrosis and nodular hyalinosis of afferent arterioles, not intimal hyperplasia, which kills option C.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.